Evidence map›Paper›PMID 29520695›Full record

ArticleMolecular and cellular biochemistry2018

AKIP1 promotes angiogenesis and tumor growth by upregulating CXC-chemokines in cervical cancer cells.

Wenying Zhang, Qiongwei Wu, Chao Wang, Longtao Yang, Ping Liu, Chengbin Ma

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.2field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 65 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Wenying ZhangGynecology Department, Changning Maternity and Infant Health Hospital, 773#, Wuyi Rd., Shanghai, 200051, China. zhangwenyingood@126.com.
Qiongwei WuGynecology Department, Changning Maternity and Infant Health Hospital, 773#, Wuyi Rd., Shanghai, 200051, China.
Chao WangGynecology Department, Changning Maternity and Infant Health Hospital, 773#, Wuyi Rd., Shanghai, 200051, China.
Longtao YangGynecology Department, Changning Maternity and Infant Health Hospital, 773#, Wuyi Rd., Shanghai, 200051, China.
Ping LiuGynecology Department, Changning Maternity and Infant Health Hospital, 773#, Wuyi Rd., Shanghai, 200051, China.
Chengbin MaGynecology Department, Changning Maternity and Infant Health Hospital, 773#, Wuyi Rd., Shanghai, 200051, China.
Shanghai Changning Maternity and Infant Health Hospital · CN

Funding

the Changning District Science and Technology Commission CNKW2015Y16
6 · The paper itself

Abstract

Upregulation of A-kinase-interacting protein 1 (AKIP1) has been observed in breast and esophageal cancers, indicating that AKIP1 may be a potent oncogenic protein. However, the role of AKIP1 in cervical cancer still remains unknown. This study aimed to explore the role of AKIP1 in cervical cancer and to investigate the underlying mechanism of AKIP1 in tumor growth. Expression of AKIP1 in cervical cancer cells was determined by qRT-PCR and western blotting. Cell-Light EdU and colony formation assays were used to determine cell proliferation. CXCL1 and CXCL8 proteins were quantified by ELISA kits. Western blotting and qRT-PCR were used to examine the alterations in signaling-related proteins and mRNA, respectively. Endothelial cell tube formation assay was performed to evaluate the effect of AKIP1 on angiogenesis. A BALB/c nude mouse xenograft model was used to evaluate the role of AKIP1 in vivo. Cancer cell proliferation was inhibited and tumor growth and angiogenesis restrained in BALB/c nude mice by suppressing AKIP1 expression in cervical cancer cell lines. In addition, overexpression of AKIP1 in cervical cancer cells elevated the levels of CXCL1, CXCL2, and CXCL8. These three chemokines were not only involved in endothelial tube formation by binding to the endothelial receptor CXCR2, but also in cervical cancer cell proliferation and clone formation, which were induced by overexpression of AKIP1. Furthermore, we found that AKIP1-induced chemokine expression was decreased by an inhibitor of nuclear factor kappa-B kinase subunit β. These results show that AKIP1 is crucial in cervical cancer angiogenesis and growth by elevating the levels of the NF-κB-dependent chemokines CXCL1, CXCL2, and CXCL8.

Indexed as

Gene Expression Regulation, NeoplasticUp-RegulationAdaptor Proteins, Signal TransducingChemokines, CXCFemaleHeLa CellsHumansNeoplasm ProteinsNeovascularization, PathologicNuclear ProteinsUterine Cervical NeoplasmsAdaptor Proteins, Signal TransducingAKIP1 protein, humanChemokines, CXCNeoplasm ProteinsNuclear ProteinsAKIP1AngiogenesisCervical cancerChemokinesIKKβ

Identifiers

PMID29520695
OpenAlexW2789443235

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.